Ask about this productRelated genes to: PDE2A antibody
- Gene:
- PDE2A NIH gene
- Name:
- phosphodiesterase 2A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-10
- Date modifiied:
- 2016-10-05
Related products to: PDE2A antibody
Related articles to: PDE2A antibody
- Diabetic cardiomyopathy (DCM) results in high mortality with surprisingly rare therapeutic approaches. Anacardic acid (AA) shows broad pharmacological properties, but its effect on DCM was unknown. This study aims to investigate the effect and molecular action of AA on DCM. KKAy mice, a model of spontaneous type 2 diabetes, were fed a high-fat diet, and were subsequently administered with AA by gavage at 5 mg/kg for 14 weeks. AA attenuated cardiac dysfunction, pathological injuries, inflammation, fibrosis, oxidative stress, and apoptosis. Mechanistically, AA was enriched in the colon, but not serum and heart, improving colonic histopathological scores, enhancing colonic tight junction protein expression and reducing serum lipopolysaccharide level, suggesting colonic epithelial barrier integrity (CEBI) as a key target of AA. In vitro experiment employed high glucose and palmitic acid-challenged colonic epithelial cells as a cell model of CEBI, showing that AA at 5 µmol/L reversed the impaired expression of tight junction proteins. RNA-sequencing identified Pde2a gene to be significantly inhibited by AA. Lentivirus-induced Pde2a overexpression in colonic epithelial cells abolished the protective effect of AA on CEBI. The present study reports that AA enhances CEBI to attenuate DCM, possibly through inhibiting colonic epithelial expression of Pde2a. - Source: PubMed
Ge RuiYin JialinMeng HualiHuang XiaoliSun LeiZheng YanYang JianjunWu Hao - - Source: PubMed
Publication date: 2026/04/02
Wen YuanZhao YuboBai Minghan - BackgroundPhysical exercise shows neuroprotective and anti-inflammatory effects in Alzheimer's disease (AD) models, but whether it modulates neuroinflammation through regulation of peripheral T-cell activity is still unresolved.ObjectiveThe present study aimed to explore the mechanisms by which aerobic exercise regulates peripheral T cell-mediated immune responses and their potential contribution to neuroinflammation in AD.MethodsMale wild-type mice and APP/PS1 transgenic mice were divided into four groups: wild-type sedentary mice (WT-SE) group, wild-type exercise group (WT-EX), APP/PS1 transgenic AD sedentary mice (AD-SE) group, and APP/PS1 transgenic AD exercise mice (AD-EX) group. The sedentary groups received no exercise training, while the exercise groups underwent a 3-month treadmill aerobic exercise intervention. At the end of the intervention, T lymphocytes were isolated from spleens. Label-free proteomics combined with LC-MS/MS was used to identify differentially expressed proteins (DEPs) and perform functional and pathway enrichment analyses. Differentially expressed protein-coding genes were validated at the mRNA level using RT-qPCR.ResultsA total of 3399 proteins were quantified across the four groups. Applying a threshold of |log fold change| > 0.67 and < 0.05, 913 DEPs were identified. These DEPs were significantly enriched in biological processes including immune system processes, protein-containing complexes, and structural molecule activity, as well as signaling pathways including AD, TGF-β, and apoptosis.ConclusionsOverall, HSP90AB1, HSP90AA1, BAG5, DNAJC8, CTSD, and ANXA1 may play a role in peripheral T-cell immune dysregulation in AD, with potential implications for central neuroinflammation. Furthermore, the beneficial effects of aerobic exercise on AD-related peripheral immune alterations, and its potential modulation of neuroinflammation, may be associated with expression changes in DEPs including Ppp2r1b, Pde2a, Casp8, Apaf-1, Dnajb11, and Dnajc13. - Source: PubMed
Publication date: 2026/03/30
Ye XingHu KaiLiu Renyi - Colorectal cancer (CRC) remains a major cause of cancer-related morbidity and mortality, with high recurrence rates and limited treatment options for metastatic disease. The tumor microenvironment (TME) and metabolic reprogramming are critical drivers of CRC progression, influencing immune responses, therapeutic resistance, and patient outcomes. - Source: PubMed
Publication date: 2026/03/09
Fu YuxiangLai JianboHuang KaibinLiu LipingLiao Guixiang - The cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway plays a central role in adrenal function, steroidogenesis, and blood pressure regulation. Increasing evidence suggests that dysregulation of this pathway contributes to several forms of hypertension, both endocrine and non-endocrine. A growing number of germline and somatic alterations affecting components of the cAMP/PKA axis have been implicated as key drivers of hypertensive disorders. Among these, activating pathogenic variants (PV) in , which encodes the stimulatory G protein α-subunit (Gsα) responsible for cAMP production, have been linked to cortisol excess. Mosaic PV , which may present with ACTH-independent Cushing syndrome, while somatic PV have been identified in cortisol-producing adrenal adenomas. Germline inactivating variants in are associated with Furthermore, germline alterations in phosphodiesterases such as and , which impair cAMP degradation, have been associated with Cushing syndrome and micronodular adrenal hyperplasia. Somatic activating PV in , the gene encoding the catalytic subunit of PKA, have also been described in cortisol-producing adenomas. In primary aldosteronism, recent studies-including data from our group-suggest that germline variants in and may contribute to bilateral adrenal hyperplasia and autonomous aldosterone production by modulating intracellular cAMP levels. Additionally, gain-of-function PV in have been associated with a familial form of salt-independent hypertension characterized by enhanced PKA signaling and vascular remodeling. This expanding body of evidence underscores the critical role of the cAMP/PKA pathway in the pathophysiology of distinct hypertensive phenotypes and highlights novel molecular mechanisms and potential therapeutic targets that merit further investigation. - Source: PubMed
Publication date: 2026/02/24
Lima Sobrinho Jose Antonio BAlmeida Madson Q